The E3 ubiquitin ligase TRAF6 controls CTLA-4 turnover and promotes T-cell-mediated antitumor immunity  

作　　者：Xiao-Liang Jie Hua Guo Guang-Biao Zhou 

机构地区：[1]State Key Laboratory of Molecular Oncology,National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital,Chinese Academy of Medical Sciences and Peking Union Medical College,100021 Bejing,China

出　　处：《Cellular & Molecular Immunology》2024年第1期97-99,共3页中国免疫学杂志（英文版）

基　　金：funded by the Key Project of the National Natural Science Foundation of China(81830093);the Non-Profit Central Research Institute Fund of CAMS(2022-RC310-05,2021-RC310-003,2020-RC310-002);CAMS Initiative for Innovative Medicine(2022-I2M-2-001);the National Natural Science Foundation of China(82372944).

摘　　要：Yu et al.[1]reported that the tumor necrosis factor(TNF)receptor OX40(CD134)-TNF receptor-associated factor 6(TRAF6)axis mediates Lys63-linked ubiquitination and subsequent lysosomal degradation of cytotoxic T-lymphocyte antigen 4(CTLA-4),leading to the enhancement of CD8^(+)T-cell-mediated antitumor immunity.Their findings unveil a previously unknown mechanism in controlling the stability of the immune checkpoint CTLA-4 and provide a potential therapeutic target for the improvement of Tcell-based immunotherapy.

关 键 词：immunity OX40 UBIQUITIN 

分 类 号：R730.3[医药卫生—肿瘤]